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WBC Path Flashcards

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1
Q

bone marrow histology

A

sinusoids lined by endothelial cells with incomplete basement membrane and adventitial cells
enter blood via transcellular migration through endo
megs-adjacent to sinusoids
erythroid surround macrophages
grans hug bony trabeculae and mature centrally

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2
Q

immature phenotyp

A

CD34

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3
Q

myeloid

A

CD13, CD33, MPO (neutrophils), CD14 ,NSE (monocytes)

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4
Q

B cell

A

CD19, CD20, kappa and lambda chain

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5
Q

T cell

A

CD1, CD3, CD4, CD7, CD8, CD5

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6
Q

causes of lymphopenia

A 
drugs-steroids, cytotoxic
systemic illness or malignancy
acute viral illness-IFN causes sequestration of T cells in LN
malnutrition
immunodef
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7
Q

neutropenia causes

A

suppression-aplastic, BM infiltrative process, infection, LGL, Kostmann syndrome (hypocellular marrow)
B12/folate deficiency, copper def, MDS, SLE, drugs, splenomegaly, overwhelming infections (hypercellular marrow)

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8
Q

consequences of neutropenia

A

mucosal ulcers-oropharynx
invasive infections of bladder and kidney and lungs
treat with GCSF

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9
Q

causes of lymphocytosis

A

transient stress-MI, seizure, trauma
drugs
viral illness-EBV, CMV, pertussis (due to toxin-unique and cool)

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10
Q

neutrophilia

A

cytokines, growth factors, and adhesion molecules

50% marginated, 50% circulating (of the 25% in blood)

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11
Q

causes of reactive neutrophilia

A

minutes-epinephrine, exercise, acute stress
hours-steroids, infection, inflammation
days-infection, GCSF tumors

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12
Q

toxic changes to neutrophils

A

granules with MPO
cytoplasmic granules
left shift
Dohle bodies

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13
Q

reactive causes of eosinophilia

A

allergic response
medication/drug hypersensitivity
connective tissue disease
parasitic infection

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14
Q

neoplastic causes of eosinophilia

A

T cell LPD
Hodgkin lymphoma
Pre-B ALL (5;14)

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15
Q

causes of monocytosis

A

infections-TB, rickettsia, malaria
inflammatory-SLE, UC
myeloid neoplasms

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16
Q

lymphadenopathy

A

lymph node enlargement

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17
Q

lymphadenitis

A

lymph node inflammation due to benign reactive process

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18
Q

causes of lymphadenopathy

A 
infections
autoimmune-RA, SLE
drugs, silicone
malignant-mets, lymphoma
sarcoid
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19
Q

follicular hyperplasia

A

B cells

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20
Q

paracortical hyperplasia

A

cellular immune response

T cell expansion

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21
Q

chromosomal abnormalities in lymphoid precursors

A

inappropriate joining of VDJ recombinase cuts

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22
Q

chromosomal abnormalities in lymphoid mature

A 
germinal B cell mutation
class switch and somatic hypermutation
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23
Q

t(14;18)

A

follicular lymphoma

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24
Q

t(8;14)

A

Burkitt lymphoma

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25
t(11;14)
mantle cell lymphoma
26
t(15;17)
acute promyelocytic leukemia
27
t(9;22)
chronic myelogenous leukemia
28
genetic instability increased risk for leukemia
Fanconi anemia Bloom syndrome Ataxia-Telangiectasia Down syndrome and neurofibromatosis I
29
HTLV-1
adult T cell leukemia/lymphoma
30
HHV8
pleural effusion lymphoma
31
EBV
Burkitt lymphoma Hodgkin lymphoma immunodeficiency associated B cell lymphomas
32
HIV
increased risk of B cell lymphomas
33
H pylori
gastric lymphomas
34
lymphoma
mostly solid organ/tissue involvement | 2/3 present with non-tender adenopathy
35
leukemia
mostly blood and/or bone marrow involvement | present with BM failure
36
plasma cell neoplasms
commonly arise in bone marrow | result in bony destruction
37
B type symptoms
fever, weight loss, night sweats
38
ALL
most common in children Caucasian>black (hispanic highest incidence) boys>girls children>adults
39
Pre B ALL
highest at 4 10,19,22 34 Tdt
40
Pre T ALL
highest at adolescence mediastinal mass 1,2,3,5,7 34 Tdt
41
clinical features of ALL
``` marrow failure sudden onset bone pain generalized adenopathy, hepatosplenomegaly CNS sx ```
42
morphology of ALL
can look similar to AML irregular contours, hand mirror no MPO (would be present in AML)
43
B ALL cytogenetics
t(12;21) ETV6 and RUNX1 | t(9;22) BCR ABL
44
T ALL cytogenetics
NOTCH
45
ALL prognosis
aggressive chemo and CNS prophylaxis children better prognosis favorable-2 to 10, low WBC, early B, trisomy 4,7,10
46
MRD
minimal residual disease | molecular detection after therapy is associated with worse outcome
47
CLL/SLL
most common leukemia of adults in the Western world | leukocytosis and mature lymphocytosis
48
clinical features CLL/SLL
>50 most are asx adenopathy, hepatosplenomegaly infections-hypogammaglobulinemia
49
CLL morphology
small mature lymphs with hyperclumped nuclear chromatin and smudge cells
50
SLL morphology
effaced, mimic germinal centers
51
immunotype CLL/SLL
CD19/5/23 | dim 20 and light chain restricted
52
CLL/SLL cytogenetics
del13q, tri12, del11q, del17p | somatic hypermutation of IGHV gene
53
CLL/SLL prognosis
``` unmutated IGHV (CD38 and ZAP70), 17p worse prognosis ```
54
Richter syndrome
transformation to DLBCL | rapidly enlarging lymph node and/or spleen
55
follicular lymphoma
NHL that mimics normal lymphoid follicles | associated with translocations involving BCL2
56
clinical features follicular lymphoma
painless adenopathy, generalized or localized BM almost always involved rarely PB involved centroblasts-mature cells used for staging paratrabecular aggregates in BM
57
diff follicular lymphoma from hyperplasia
no polarization no tingable bodies reverse BCL2 staining
58
immunophenotype follicular lymphoma
CD19/20/10
59
prognosis follicular lymphoma
incurable but indolent | transformation to high grade or DLBCL
60
mantle cell lymphoma
resembles normal mantle zone cells | tumor cells aberrantly expressed CD5 and overexpress cyclin D1
61
clinical features of mantle cell lymphoma
painless, generalized lymphadenopathy BM involvement in most lymphomatoid polyposis=GI involvement blastoid variant is more aggressive
62
immunotype mantle cell lymphoma
19/20/5 | bright surface light chain
63
prognosis mantle cell lymphoma
not curable Rituximab indication for BM transplant
64
marginal zone lymphoma
mostly extranodal | tumor cell resembles marginal zone cell-post germinal center memory B cell
65
clinical features of marginal zone lymphoma
``` arise in tissues from chronic inflammatory disorders h. pylori hashimoto Sjogren small bowel lung may regress if brought under control ```
66
cytogenetics of marginal zone lymphoma
polyclonal to oligoclonal to monoclonal | acquisition of t(11;18) or t(1;14) with upregulation of BCL10 or MALT1 now independent of extrinsic stimuli
67
morphology of marginal zone lymphoma
pleomorphic population of monoxytoid B cells and plasmacytoid cells
68
DLBCL
high grade most common type of NHL most patients lack specific risk factor
69
clinical features of DLBCL
rapidly enlarging symptomatic mass nodal or extranodal B symptoms BM involvement occurs late in disease
70
morphology of DLBCL
convoluted nuclear contours 1-3 nucleoli mitotically active
71
cytogenetics DLBCL
BCL6 BCL2 MYC
72
immunotype DLBCL
CD19/20 | light chain restriction
73
prognosis DLBCL
ABC subtype is poor prognostic indicator aggressive and fatal if untreated RCHOP
74
Burkitt lymphoma
high grade African-EBV associated Sporadic in children (20% EBV associated) usually extranodal (abdominal mass in sporadic and mandibular in endemic)
75
Tumor lysis syndrome
rapid cell turnover tumor cell death releases uric acid, potassium, calcium medical emergency requiring hydration CNS disease occurs in most patients
76
morphology of Burkitt lymphoma
basophilic cytoplasm with vacuoles high mitotic Ki-67 macrophages-starry sky
77
immunotype Burkitt lymphoma
19/20/10 surface light chain restriction bcl6 Ki67
78
cytogenetics Burkitt lymhoma
t(8;14) t(2;8) t(8;22)
79
plasma cell neoplasms
clonal plasma cell proliferation | M protein, Bence Jones protein
80
Bence Jones protein
monoclonal free light chain in urine
81
M protein
monoclonal protein secreted by plasma cell and identified in blood
82
multiple myeloma
clonal plasma cells secrete M protein into blood or urine and cause end organ damage
83
pathogenesis multiple myeloma
translocations involving IgH and cyclins tumors produce IL6 activate osteoclasts/inhibit osteoblasts hypercalcemia IgG>A>M inadequate normal immunoglobulin production
84
clinical presentation of multiple myeloma
``` weakenss-anemia infections-decreased normal Ig polyuria-hypercalcemia bone pain renal insufficiency-Bence Jones amyloidosis-light chain deposition in organs ```
85
roleaux
multiple myeloma blood smear | incrased protein causes them to clump like a stack of coins
86
smoldering myeloma
>10% clonal bone marrow plasma cells absence of end organ damage can progress to myeloma
87
prognosis of multiple myeloma
death from infections and renal failure | nothing is curative
88
MGUS
monoclonal gammopathy | periodic assessment of BJ protein and M protein to check for progression to MM
89
plasmacytoma
solitary bone or soft tissue clonal plasma cell masses with no evidence of marrow or organ disease can progress to myeloma local field radiation therapy
90
lymphoplasmacytic lymphoma (LPL)
monoclonal IgM causing hyperviscosity syndrome called Waldenstrom macroglobinemia no light chain deposition and no bony lesions resembles SLL
91
Waldenstrom macroglobinemia
IgM increase viscosity visual sx, neurologic sx, bleeding, cryoglobulinemia plasmapheresis to alleviate sx
92
mutation for LPL
MYD88
93
Hariy Cell leukemia
older male with splenomegaly and pancytopenia | BRAF mutation
94
clinical featues of HCL
symptoms from cytopenias and splenomegaly spleen and BM involvement monocytopenia
95
dry tap in HCL
due to increased reticulin fibrosis
96
immunotype HCL
19/20/light chain restricted | 11/25/103
97
prognosis HCL
sensitive to purine analogs (cladribine) | BRAF inhibitors
98
mature T cell neoplasms
aberrant T cell phenotype PCR required to ID rearrangement of TCR
99
peripheral T cell lymphoma not otherwise specified
eosinophilia pruritis, fever, weight loss woser than B cell
100
anaplastic large cell lymphoma
translocation involving ALK found in kids morphology-horseshoe or wreath shaped nuclei
101
adult t cell leukemia/lymphoma
retrovirus HTLV1 CD4 T cells infected leukemic-rapidly progressive skin localized is less aggressive
102
mycosis fungoides/sezary syndrome
CD4 helper T cells that home to skin MF as patch, plaque, tumor SS-exfoliative erythroderma plus leukemia
103
appearance of MF/SS
cerebriform nuclear contours
104
prognosis of MF/SS
indolent if <10% skin lifespan unaffected | mortality from immunodef
105
large granular lymphocytic leukemia
STAT3 mutations minimal BM infiltration but neutropenia and anemia T/NK associated with Felty syndrome
106
Felty syndrome
rheumatoid arthritis-autoimmunity provoked by neoplastic cells neutropenia splenomegaly-infiltrates in the spleen
107
Hodgkin lymphoma
``` classical (Reed Sternberg) nodular sclerosing-most common mixed cellularity lymphocyte rich lymphocyte depleted nodular lymphocyte predominance-LP cell (popcorn cell) ```
108
Hodgkin lymphoma vs NHL
``` arises in single node spreads in contiguous fashion neoplastic cell is Reed Sternberg cell-minority of population, reactive cells recruited by cytokines bimodal-young adults and peak at 45 usually curable with radiation and chemo ```
109
Reed Sternberg cell
derived from germinal center or post germinal center B cells | RS in individual have identical rearranged Ig genes-somatic hypermutation
110
classic RS immunotype
30/15
111
NLPHL RS immunotype
20/45
112
presentation of Hodgkin lymphoma
painless localized or generalized adenopathy mediastinal enlargment long term survivors have increased risk of secondary malignancies
113
NSHL
70% of cases cervical, supraclavicular and mediastinal nodes lacunar cell and bands of polarizing fibrosis
114
MCHL
mixed cellularity associated with EBV B signs advanced stage
115
myeloproliferative neoplasms
effective hematopoiesis just too much of it no dysplasia multipotent can give rise to all myeloid (CML it is pluripotent so it can give rise to myeloid and lymphoid lines)
116
MPN
``` BCR ABL JAK2 MPL CALR PDGFR alpha ```
117
CML
pluripotent stem cell abnormality | t(9;22) BCR ABL for Philadelphia chromosome
118
CML morphology
leukocytosis with left shift eosinophilia and basophila packed BM with sea blue histiocytes splenomegaly due to EMH
119
clinical features of CML
middle age EMH-LUQ pain slow progression (chronic to accelerated blast)
120
CML treatment
Imantinib | resistance can occur in subclones-does not eliminate the clone
121
PV
must rule out secondary polycythemia decreased EPO JAK2 mutation
122
causes of secondary polycythemia
``` increased EPO high altitude chronic hypoxic disorders hemoglobinopathies renal transplant neoplasm-uterine, renal, cerebellar, ovarian, hepatoma, pheo ```
123
PV clinical features
``` late middle age sx from increased RBC mass hyperuricemia due to high cell turnover bleeding and thrombosis-abnormal places acquired von Willebrand minimal reticulin fibrosis ```
124
ET
platelet count with abnormal large platelets sustained thrombocytosis in blood-increased large mature megs JAK2
125
diagnosis of ET
exclusion | must rule out reactive, IDA, inflammation, asplenism
126
clinical ET
thrombosis | bleeding-acquired von Willebrand syndrome
127
treatment of ET
hydroxyurea (also used to treat sickle)
128
PM
neoplastic megs release PDGF and TGF beta which are fibroblast mitogen increased reticulin and collagen fibrosis JAK2
129
phases of PM
pre fibrotic-thrombocytosis could be ET or reactive | fibrotic-anemia, early satiety
130
MDS
depends on blast count | clonal stem cell abnormality resulting in ineffective hematopoiesis with dysplasia
131
MDS morphology
PB-cytopenic with anemia, dysplasic neutrophils, platelets BM-hypercellular, blasts<20% increase in iron storage
132
MDS genetics
5,7
133
MDS treatment
supportive care with transfusions, antibiotics Vidaza Allo-stem cell transplant
134
AML-myeloblast
Auer rods 34/13/33 MPO positive
135
AML-monoblast
11/14/33/64 | NSE positive
136
AML pathophysiology
acquired genetic alteration-RUNX1, RARA mutation in signal transduction-JAK2 >20% blasts hypercellular leads to pancytopenia
137
AML presentation
due to bone marrow failure fatigue, pallor-anemia bruising and petechiae-thrombocytopenia infections-neutropenia
138
granulocytic sarcoma
tissue mass of blasts in absence of PB or BM involvement (will progress to AML if left untreated)
139
AML with recurrent cytogenetic abnormalities
Acute promyelocytic leukemia associated with DIC RARA (15;17)
140
AML with gene mutations
NPM1
141
AML with myelodysplasia related change
poor prognosis-behaving aggressively
142
Splenomegaly
HCL, primary fibrotic hyperplasia LUQ dragging sensation discomfort after eating
143
nonspecific acute splenitis
blood borne infection softness congestion of red pulp
144
congestive splenomegaly-intrahepatic
RHF | hepatic cirrhosis
145
congestive splenomegaly-extrahepatic
spontaneous portal vein thrombosis | splenic vein thrombosis
146
pathologic findings of splenomegaly
firmness | sugar coating
147
splenic infarcts
pale, wedge shaped and subcapsular in location | associated with infective endocarditis
148
accessory spleen
in gastrosplenic ligament, tail of pancreas, omentum, large/small bowel mesenteries only important in hereditary spherocytosis-becomes dominant spleen if not removed
149
thymic hyperplasia
secondary follicles | associated with myasthenia gravis, graves, SLE, RA
150
thymoma
tumor of epithelial cells with background of immature T cells anterior superior mediastinum of adults
151
benign thymoma
encapsulated | medullary or mixed medullary and cortical epithelial cells
152
malignant thymomas
cytologically benign but invasive-cortical epithelial cells | cytologically malignant-squamous cell carcinoma, lymphoepithelioma EBV
153
langerhans cell histiocytosis
tumor from dendritic cells express HLA-DR, S-100, CD1 Birbeck granules tennis racket on EM

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